Rapid cooling contracture with cold cardioplegia.
Rapid cooling contracture with cold cardioplegia.
复制标题
用冷停跳液快速冷却挛缩。
DOI：
10.1016/s0003-4975(97)00087-8
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Daggett,WM
中科院分区：
文献类型：
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作者：
Lahorra,JA;Torchiana,DF;TolisJr,G;Bashour,CA;Hahn,C;Titus,JS;Geffin,GA;Daggett,WM
冷停搏液可引起快速冷却挛缩。心脏停搏液诱导的冷却挛缩与心肌温度或心肌细胞钙的关系尚不清楚。方法：在4°、20°和37°C随机顺序灌注3次心脏停搏液（1 mmol/L钙），每次2 min，然后在37°C下搏动10 min。最后，通过在37°C下输注1分钟心脏停搏液进行热诱导停搏，然后在4°C下输注1分钟。Indo-1用于测量其中6个心脏中的细胞内Ca 2+浓度。另外的心脏在4°或37°C下接受缺氧、无葡萄糖的心脏停搏液。在4°、20°和37°C下心脏停搏1分钟后，左心室发展压力迅速上升至其停搏前值的54% ± 3%、43% ± 3%和18% ± 1%，而细胞内Ca 2+浓度达到166% ± 23%、94% ± 4%、94% ± 4%。和37% ± 10%的停搏前瞬变。冠脉流量分别为5.7 ± 0.2、8.7 ± 0.3和12.6 ± 0.6 mL/min。在37°C的温停搏液诱导下，在随后的4°C停搏液中，左心室发展压力和[Ca 2 +]分别降低了16%（p = 0.001）和34%（p = 0.03）。腺苷三磷酸和磷酸肌酸含量低于后4°C比37°C缺氧，无葡萄糖cardioparalys.CONCLUSIONSRapid冷却期间cardioparalys. Rapid冷却增加左心室压力，[Ca 2 +]i，和冠状动脉阻力，是能量消耗。没有快速冷却挛缩可能是暖心手术和心脏停搏液热诱导的益处。
BACKGROUNDCold cardioplegia can induce rapid cooling contracture. The relations of cardioplegia-induced cooling contracture to myocardial temperature or myocyte calcium are unknown.METHODSTwelve crystalloid-perfused isovolumic rat hearts received three 2-minute cardioplegic infusions (1 mmol/L calcium) at 4°, 20°, and 37°C in random order, each followed by 10 minutes of beating at 37°C. Finally, warm induction of arrest by a 1-minute cardioplegic infusion at 37°C was followed by a 1-minute infusion at 4°C. Indo-1 was used to measure the intracellular Ca2+concentration in 6 of these hearts. Additional hearts received hypoxic, glucose-free cardioplegia at 4° or 37°C.RESULTSAfter 1 minute of cardioplegia at 4°, 20°, and 37°C, left ventricular developed pressure rose rapidly to 54% ± 3%, 43% ± 3%, and 18% ± 1% of its prearrest value, whereas the intracellular Ca2+concentration reached 166% ± 23%, 94% ± 4%, and 37% ± 10% of its prearrest transient. Coronary flow was 5.7 ± 0.2, 8.7 ± 0.3, and 12.6 ± 0.6 mL/min, respectively. Warm cardioplegia induction at 37°C reduced left ventricular developed pressure and [Ca2+]iduring subsequent 4°C cardioplegia by 16% (p = 0.001) and 34% (p = 0.03), respectively. Adenosine triphosphate and phosphocreatine contents were lower after 4°C than after 37°C hypoxic, glucose-free cardioplegia.CONCLUSIONSRapid cooling during cardioplegia increases left ventricular pressure, [Ca2+]i, and coronary resistance, and is energy consuming. The absence of rapid cooling contracture may be a benefit of warm heart operations and warm induction of cardioplegic arrest.